Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

2008 ◽  
Vol 295 (5) ◽  
pp. R1613-R1622 ◽  
Author(s):  
Philip N. Ainslie ◽  
Michael Hamlin ◽  
John Hellemans ◽  
Peter Rasmussen ◽  
Shigehiko Ogoh
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Hypoxic Exercise

We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.

Influence of sympathoexcitation at high altitude on cerebrovascular function and ventilatory control in humans

2012 ◽  
Vol 113 (7) ◽  
pp. 1058-1067 ◽  
Author(s):  
P. N. Ainslie ◽  
S. J. E. Lucas ◽  
J.-L. Fan ◽  
K. N. Thomas ◽  
J. D. Cotter ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Adrenergic Blockade ◽  
Ventilatory Control ◽  
Phase Lead ◽  
Arterial Blood ◽  
Transfer Function Analysis

We sought to determine the influence of sympathoexcitation on dynamic cerebral autoregulation (CA), cerebrovascular reactivity, and ventilatory control in humans at high altitude (HA). At sea level (SL) and following 3–10 days at HA (5,050 m), we measured arterial blood gases, ventilation, arterial pressure, and middle cerebral blood velocity (MCAv) before and after combined α- and β-adrenergic blockade. Dynamic CA was quantified using transfer function analysis. Cerebrovascular reactivity was assessed using hypocapnia and hyperoxic hypercapnia. Ventilatory control was assessed from the hypercapnia and during isocapnic hypoxia. Arterial Pco2 and ventilation and its control were unaltered following blockade at both SL and HA. At HA, mean arterial pressure (MAP) was elevated ( P < 0.01 vs. SL), but MCAv remained unchanged. Blockade reduced MAP more at HA than at SL (26 vs. 15%, P = 0.048). At HA, gain and coherence in the very-low-frequency (VLF) range (0.02–0.07 Hz) increased, and phase lead was reduced (all P < 0.05 vs. SL). Following blockade at SL, coherence was unchanged, whereas VLF phase lead was reduced (−40 ± 23%; P < 0.01). In contrast, blockade at HA reduced low-frequency coherence (−26 ± 20%; P = 0.01 vs. baseline) and elevated VLF phase lead (by 177 ± 238%; P < 0.01 vs. baseline), fully restoring these parameters back to SL values. Irrespective of this elevation in VLF gain at HA ( P < 0.01), blockade increased it comparably at SL and HA (∼43–68%; P < 0.01). Despite elevations in MCAv reactivity to hypercapnia at HA, blockade reduced ( P < 0.05) it comparably at SL and HA, effects we attributed to the hypotension and/or abolition of the hypercapnic-induced increase in MAP. With the exception of dynamic CA, we provide evidence of a redundant role of sympathetic nerve activity as a direct mechanism underlying changes in cerebrovascular reactivity and ventilatory control following partial acclimatization to HA. These findings have implications for our understanding of CBF function in the context of pathologies associated with sympathoexcitation and hypoxemia.

Impaired cerebral haemodynamic function associated with chronic traumatic brain injury in professional boxers

2012 ◽  
Vol 124 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Damian M. Bailey ◽  
Daniel W. Jones ◽  
Andrew Sinnott ◽  
Julien V. Brugniaux ◽  
Karl J. New ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Function Analysis ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Mechanical Trauma ◽  
Neurocognitive Dysfunction ◽  
Arterial Blood ◽  
Transfer Function Analysis

The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO2 (cerebrovascular reactivity to changes in CO2: 5% CO2 and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitive function (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial blood pressure (finger photoplethysmography), end-tidal CO2 (capnography) and cortical oxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (P<0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lower CVRCO2 range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r=−0.84, P<0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career.

Cerebrovascular reactivity and dynamic autoregulation in tetraplegia

2010 ◽  
Vol 298 (4) ◽  
pp. R1035-R1042 ◽  
Author(s):  
Luke C. Wilson ◽  
James D. Cotter ◽  
Jui-Lin Fan ◽  
Rebekah A. I. Lucas ◽  
Kate N. Thomas ◽  
...  
Keyword(s):  
Transfer Function ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Cardiovascular Function ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Cord Injury

Humans with spinal cord injury have impaired cardiovascular function proportional to the level and completeness of the lesion. The effect on cerebrovascular function is unclear, especially for high-level lesions. The purpose of this study was to evaluate the integrity of dynamic cerebral autoregulation (CA) and the cerebrovascular reactivity in chronic tetraplegia (Tetra). After baseline, steady-state hypercapnia (5% CO2) and hypocapnia (controlled hyperventilation) were used to assess cerebrovascular reactivity in 6 men with Tetra (C5–C7 lesion) and 14 men without [able-bodied (AB)]. Middle cerebral artery blood flow velocity (MCAv), cerebral oxygenation, arterial blood pressure (BP), heart rate (HR), cardiac output (Q̇; model flow), partial pressure of end-tidal CO2 (PetCO2), and plasma catecholamines were measured. Dynamic CA was assessed by transfer function analysis of spontaneous fluctuations in BP and MCAv. MCAv pulsatility index (MCAv PI) was calculated as (MCAvsystolic − MCAvdiastolic)/MCAvmean and standardized by dividing by mean arterial pressure (MAP). Resting BP, total peripheral resistance, and catecholamines were lower in Tetra ( P < 0.05), and standardized MCAv PI was ∼36% higher in Tetra ( P = 0.003). Resting MCAv, cerebral oxygenation, HR, and PetCO2 were similar between groups ( P > 0.05). Although phase and transfer function gain relationships in dynamic CA were maintained with Tetra ( P > 0.05), coherence in the very low-frequency range (0.02–0.07 Hz) was ∼21% lower in Tetra ( P = 0.006). Full (hypo- and hypercapnic) cerebrovascular reactivity to CO2 was unchanged with Tetra ( P > 0.05). During hypercapnia, standardized MCAv PI reactivity was enhanced by ∼78% in Tetra ( P = 0.016). Despite impaired cardiovascular function, chronic Tetra involves subtle changes in dynamic CA and cerebrovascular reactivity to CO2. Changes are evident in coherence at baseline and MCAv PI during baseline and hypercapnic states in chronic Tetra, which may be indicative of cerebrovascular adaptation.

Assessment of cerebral autoregulation: the quandary of quantification

2012 ◽  
Vol 303 (6) ◽  
pp. H658-H671 ◽  
Author(s):  
Y. C. Tzeng ◽  
P. N. Ainslie ◽  
W. H. Cooke ◽  
K. C. Peebles ◽  
C. K. Willie ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Transfer Function ◽  
Cerebral Autoregulation ◽  
Convergent Validity ◽  
Function Analysis ◽  
Pressure Fluctuations ◽  
Low Frequency ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Normalized Gain

We assessed the convergent validity of commonly applied metrics of cerebral autoregulation (CA) to determine the extent to which the metrics can be used interchangeably. To examine between-subject relationships among low-frequency (LF; 0.07–0.2 Hz) and very-low-frequency (VLF; 0.02–0.07 Hz) transfer function coherence, phase, gain, and normalized gain, we performed retrospective transfer function analysis on spontaneous blood pressure and middle cerebral artery blood velocity recordings from 105 individuals. We characterized the relationships ( n = 29) among spontaneous transfer function metrics and the rate of regulation index and autoregulatory index derived from bilateral thigh-cuff deflation tests. In addition, we analyzed data from subjects ( n = 29) who underwent a repeated squat-to-stand protocol to determine the relationships between transfer function metrics during forced blood pressure fluctuations. Finally, data from subjects ( n = 16) who underwent step changes in end-tidal Pco2 (PetCO2) were analyzed to determine whether transfer function metrics could reliably track the modulation of CA within individuals. CA metrics were generally unrelated or showed only weak to moderate correlations. Changes in PetCO2 were positively related to coherence [LF: β = 0.0065 arbitrary units (AU)/mmHg and VLF: β = 0.011 AU/mmHg, both P < 0.01] and inversely related to phase (LF: β = −0.026 rad/mmHg and VLF: β = −0.018 rad/mmHg, both P < 0.01) and normalized gain (LF: β = −0.042%/mmHg2 and VLF: β = −0.013%/mmHg2, both P < 0.01). However, PetCO2 was positively associated with gain (LF: β = 0.0070 cm·s−1·mmHg−2, P < 0.05; and VLF: β = 0.014 cm·s−1·mmHg−2, P < 0.01). Thus, during changes in PetCO2, LF phase was inversely related to LF gain (β = −0.29 cm·s−1·mmHg−1·rad−1, P < 0.01) but positively related to LF normalized gain (β = 1.3% mmHg−1/rad, P < 0.01). These findings collectively suggest that only select CA metrics can be used interchangeably and that interpretation of these measures should be done cautiously.

Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration

2008 ◽  
Vol 105 (2) ◽  
pp. 433-445 ◽  
Author(s):  
Jui-Lin Fan ◽  
James D. Cotter ◽  
Rebekah A. I. Lucas ◽  
Kate Thomas ◽  
Luke Wilson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Regional Differences ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Blood Flows ◽  
Time Control ◽  
Arterial Blood ◽  
Cerebrovascular Function ◽  
End Tidal ◽  
Passive Hyperthermia

The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q̇) would compromise blood flow velocity in the middle cerebral artery (MCAv) and cerebral oxygenation; 2) Hypo would exacerbate the hyperthermic-induced hypocapnia, further decreasing MCAv; and 3) heating would reduce MCAv-CO2 reactivity, thereby altering ventilation. Ten men, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5°C increments in core (esophageal) temperature (TC) to +2°C] while euhydrated (Euh) or Hypo by 1.5% body mass (attained previous evening). Time-control (i.e., non-heat stressed) data were obtained on six of these subjects. Cerebral oxygenation (near-infrared spectroscopy), MCAv, end-tidal carbon dioxide (PetCO2) and arterial blood pressure, Q̇ (flow model), and brachial and carotid blood flows (CCA) were measured continuously each 0.5°C change in TC. At each level, hypercapnia was achieved through 3-min administrations of 5% CO2, and hypocapnia was achieved with controlled hyperventilation. At baseline in Hypo, heart rate, MCAv and CCA were elevated ( P < 0.05 vs. Euh). MCAv-CO2 reactivity was unchanged in both groups at all TC levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in PetCO2 (−8 ± 1 mmHg/°C), which was related to lower MCAv (−15 ± 3%/°C; R2 = 0.98; P < 0.001). Elevations in Q̇ were related to increases in brachial blood flow ( R2 = 0.65; P < 0.01) and reductions in MCAv ( R2 = 0.70; P < 0.01), reflecting peripheral distribution of Q̇. Cerebral oxygenation was maintained, presumably via enhanced O2-extraction or regional differences in cerebral perfusion.

Resistance but not endurance exercise training induces changes in cerebrovascular function in healthy young subjects

2021 ◽  
Author(s):  
Hannah J. Thomas ◽  
Channa E. Marsh ◽  
Louise H. Naylor ◽  
Philip N. Ainslie ◽  
Kurt J. Smith ◽  
...  
Keyword(s):  
Resistance Training ◽  
Arterial Pressure ◽  
Endurance Training ◽  
Acute Exercise ◽  
Internal Carotid ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Brain Health ◽  
Cerebrovascular Resistance ◽  
Cerebrovascular Function

Aim: It is generally considered that regular exercise maintains brain health and reduces the risk of cerebrovascular diseases such as stroke and dementia. Since the benefits of different 'types' of exercise are unclear, we sought to compare the impacts of endurance and resistance training on cerebrovascular function. Methods: In a randomized and cross-over design, 68 young healthy adults were recruited to participate in 3-months of resistance and endurance training. Cerebral hemodynamics through the internal carotid, vertebral, middle and posterior cerebral arteries were measured using Duplex ultrasound and transcranial Doppler at rest and during acute exercise, dynamic autoregulation and cerebrovascular reactivity (to hypercapnia). Results: Following resistance, but not endurance training, middle cerebral artery velocity and pulsatility index significantly decreased (P<0.01 and P=0.02, respectively), while mean arterial pressure and cerebrovascular resistance in the middle, posterior and internal carotid arteries all increased (P<0.05). Cerebrovascular resistance in response to acute exercise and hypercapnia also significantly increased following resistance (P=0.02), but not endurance training. Conclusions: Our findings, which were consistent across multiple domains of cerebrovascular function, suggest that episodic increases in arterial pressure associated with resistance training may increase cerebrovascular resistance. The implications of long-term resistance training on brain health require future study, especially in populations with pre-existing cerebral hypoperfusion and/or hypotension.

Dynamic modulation of cerebrovascular resistance as an index of autoregulation under tilt and controlled Pet CO2

2002 ◽  
Vol 283 (3) ◽  
pp. R653-R662 ◽  
Author(s):  
Michael R. Edwards ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson
Keyword(s):  
Transfer Function ◽  
Function Analysis ◽  
Low Frequency ◽  
Mean Flow ◽  
Low Frequencies ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Frequency Changes

Transfer function analysis of the arterial blood pressure (BP)-mean flow velocity (MFV) relationship describes an aspect of cerebrovascular autoregulation. We hypothesized that the transfer function relating BP to cerebrovascular resistance (CVRi) would be sensitive to low-frequency changes in autoregulation induced by head-up tilt (HUT) and altered arterial Pco 2. Nine subjects were studied in supine and HUT positions with end-tidal Pco 2(Pet CO2 ) kept constant at normal levels: +5 and −5 mmHg. The BP-MFV relationship had low coherence at low frequencies, and there were significant effects of HUT on gain only at high frequencies and of Pco 2 on phase only at low frequencies. BP → CVRi had coherence >0.5 from very low to low frequencies. There was a significant reduction of gain with increased Pco 2 in the very low and low frequencies and with HUT at the low frequency. Phase was affected by Pco 2 in the very low frequencies. Transfer function analysis of BP → CVRi provides direct evidence of altered cerebrovascular autoregulation under HUT and higher levels of Pco 2.

scholarly journals N‐Terminal Pro Brain, N‐Terminal Pro Atrial Natriuretic Peptides, and Dynamic Cerebral Autoregulation

2020 ◽  
Vol 9 (20) ◽  
Author(s):  
Simin Mahinrad ◽  
Behnam Sabayan ◽  
Chaney R. Garner ◽  
Donald M. Lloyd‐Jones ◽  
Farzaneh A. Sorond
Keyword(s):  
Natriuretic Peptides ◽  
Cerebral Autoregulation ◽  
Small Vessel Disease ◽  
Function Analysis ◽  
Transcranial Doppler Ultrasound ◽  
Linear Regression Models ◽  
Lower Phase ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
Dynamic Cerebral Autoregulation

Background Elevated natriuretic peptides (NP) are associated with adverse cerebrovascular conditions including stroke, cerebral small vessel disease, and dementia. However, the mechanisms underlying these associations remain unclear. In this study, we examined the relationship of NT‐proBNP (N‐terminal pro brain NP) and NT‐proANP (N‐terminal pro atrial NP) with cerebrovascular function, measured by cerebral autoregulation. Methods and Results We included 154 participants (mean age 56±4 years old) from the CARDIA (Coronary Artery Risk Development in Young Adults) cohort. NT‐proBNP and NT‐proANP were measured in blood samples from the year 25 examination using electrochemiluminescence Immunoassay and enzyme‐linked immunoassay, respectively. Dynamic cerebral autoregulation (dCA) was assessed at the year 30 examination by transcranial Doppler ultrasound, using transfer function analysis (phase and gain) of spontaneous blood pressure and flow velocity oscillations, where lower phase and higher gain reflect less efficient cerebral autoregulation. We used multivariable linear regression models adjusted for demographics, vascular risk factors, and history of kidney and cardiac diseases. Higher NT‐proBNP levels at year 25 were associated with lower phase (β [95% CI]=−5.30 lower degrees of phase [−10.05 to −0.54]) and higher gain (β [95% CI]=0.06 higher cm/s per mm Hg of gain [0.004–0.12]) at year 30. Similarly, higher NT‐proANP levels were associated with lower phase (β [95% CI]=−9.08 lower degrees of phase [−16.46 to −1.70]). Conclusions Higher circulating levels of NT‐proBNP and NT‐proANP are associated with less efficient dCA 5 years later. These findings link circulating NP to cerebral autoregulation and may be one mechanism tying NP to adverse cerebrovascular outcomes.

Accuracy of a Cerebral Oximeter in Healthy Volunteers under Conditions of Isocapnic Hypoxia 

1998 ◽  
Vol 88 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Lindsey C. Henson ◽  
Carolyn Calalang ◽  
John A. Temp ◽  
Denham S. Ward
Keyword(s):  
Infrared Spectroscopy ◽  
Oxygen Saturation ◽  
Healthy Volunteers ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Jugular Bulb ◽  
Wide Range ◽  
Cerebral Oximeter ◽  
End Tidal

Background A cerebral oximeter measures oxygen saturation of brain tissue noninvasively by near infrared spectroscopy. The accuracy of a commercially available oximeter was tested in healthy volunteers by precisely controlling end-tidal oxygen (P[ET]O2) and carbon dioxide (P[ET]CO2) tensions to alter global cerebral oxygen saturation. Methods In 30 healthy volunteers, dynamic end-tidal forcing was used to produce step changes in P[ET]O2 resulting in arterial saturation ranging from approximately 70% to 100% under conditions of controlled normocapnia (each person's resting P[ET]CO2) or hypercapnia (resting plus 7-10 mmHg). Blood arterial (SaO2) and jugular bulb venous (S[jv]O2) saturations during each P(ET)O2 interval were determined by co-oximetry. The cerebral oximeter reading (rSO2) and an estimated jugular venous saturation (S[jv]O2), derived from a combination of SaO2 and rSO2, were compared with the measured S(jv)O2. Results The S(jv)O2 was significantly higher with hypercapnia than with normocapnia for the same SaO2. The rSO2 and S(jv)O2 were both highly correlated with S(jv)O2 for individual volunteers (mean r2 = 0.91 for each relation); however, the slopes and intercepts varied widely among volunteers. In three of them, the cerebral oximeter substantially underestimated the measured S(jv)O2. Conclusions During isocapnic hypoxia in healthy persons, cerebral oxygenation as estimated by near infrared spectroscopy precisely tracks changes in measured S(jv)O2 within individuals, but the relation exhibits a wide range of slopes and intercepts. Therefore the clinical utility of the device is limited to situations in which tracking trends in cerebral oxygenation would be acceptable.

Effects of hyperglycemia on the cerebrovascular response to rhythmic handgrip exercise

2007 ◽  
Vol 293 (1) ◽  
pp. H467-H473 ◽  
Author(s):  
Yu-Sok Kim ◽  
Rikke Krogh-Madsen ◽  
Peter Rasmussen ◽  
Peter Plomgaard ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Function Analysis ◽  
Low Frequency ◽  
Resistance Index ◽  
Handgrip Exercise ◽  
Dynamic Relationship ◽  
Hyperglycemic Clamp ◽  
Transfer Function Analysis

Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity ( Vmean) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU ( P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA Vmean increased ( P < 0.05), whereas brain catecholamine uptake and arterial Pco2 did not change significantly. HY did not affect the normalized low-frequency gain between mean arterial pressure and MCA Vmean or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 ± 7% vs. 9 ± 7%; P < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 ± 4% vs. 14 ± 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA Vmean. These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise.

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